Prevalence of sarcopenia according to EWGSOP1 and EWGSOP2 in older adults and their associations with unfavorable health outcomes: a systematic review.

BACKGROUND: The European Working Group on Sarcopenia in Older People (EWGSOP) recently updated the definition and diagnostic criteria to assess sarcopenia, which can result in important changes in sarcopenia prevalence in older adults. AIM: To compare the prevalence of sarcopenia through the diagnostic criteria and definition proposed by the first (EWGSOP1) and recent (EWGSOP2) European consensus in older adults. We also aimed to evaluate which sarcopenia consensus is better associated with unfavorable health outcomes. METHODS: The review followed PRISMA guidelines. Embase, Medline (PubMed), Scopus and Web of Science were searched from 2018 to February 2021. The systematic review protocol was registered at PROSPERO (CRD42020213303). The search, selection, and evaluation processes were done in a duplicate and independent manner. RESULTS: Of the 298 potentially eligible articles, 9 were included in this review. The prevalence of sarcopenia was 17.7% by EWGSOP1 and 11% by EWGSOP2. Evaluating all the studies, the sarcopenia prevalence ranged from 6.2 to 35.3% for the EWGSOP1, and from 3.2 to 26.3% for the EWGSOP2. Five studies have evaluated the association between the prevalence of sarcopenia (EWGSOP1 versus EWGSOP2) and unfavorable health outcomes, in which three studies showed that EWGSOP1 was better associated with increased risk of hospitalization and/or mortality. CONCLUSION: In comparison with EWGSOP1, the prevalence of sarcopenia in older adults decreased when diagnosed according to EWGSOP2. Based on limited evidence, EWGSOP2 seems to be worse for predicting unfavorable outcomes compared with EWGSOP1.

Enzymatic Modulators from Induratia spp.

In the present work, ethyl acetate extracts, consisting of non-volatile compounds, from the culture of endophytic fungi isolated from coffee plants, Induratia coffeana and Induratia yucatanensis, were prospected in enzyme modulation tests that act in human hemostasis. Dry extracts of the fungi were diluted in dimethyl sulfoxide p.a. 99.9% (DMSO), and then tested. Bothrops atrox venom was used as an enzyme source and tool to induce the activities. Prior to the evaluation of the activities, incubations of the extracts with the venom were performed in the proportions 1: 0.01, 1: 0.25, 1: 0.5, and 1: 1 (venom: extract; mass: mass). The extracts of all fungi promoted a significant increase in the clotting time induced by the venom, which was even longer when the extracts were previously incubated with the citrated plasma. The activity of phospholipases A2 did not significantly change when evaluated in the presence of fungal extracts. However, the evaluated extracts inhibited proteases by 73% and 30% in the thrombolytic and caseinolytic tests, respectively. In addition, the extracts did not induce cytotoxicity on human erythrocytes when evaluated in the absence of the venom. Thus, it is possible to suggest the presence of specific interactions between molecules present in extracts of Induratia spp. and venom proteases, highlighting non-volatile metabolites as promising sources of compounds of medical and scientific interest.

Obesity-like metabolic effects of high-carbohydrate or high-fat diets consumption in metabolic and renal functions.

Present study investigated which diet, high-carbohydrate (HCD) or high-fat (HFD), most effectively induces classical characteristics of obesity in mice. Mice were fed commercial chow (control), an HCD, or an HFD for 12 weeks. HFD and HCD increased body weight, fat mass, and glycaemia, whereas the HFD augmented insulinemia. In the kidney, the HFD caused albuminuria, and reductions in fractional Na+ excretion, Thromboxane B2 (TXB2) excretion, and urinary flow, whereas the HCD reduced glomerular filtration, plasma osmolality, and TXB2 and Prostaglandin E2 excretion. The consumption of HFD and HCD modified parameters that indicate histopathological changes, such as proliferation (proliferating-cell-nuclear antigen), inflammation (c-Jun N-terminal-protein), and epithelial-mesenchymal transition (vimentin, and desmin) in renal tissue, but the HCD group presents fewer signals of glomerular hypertrophy or tubule degeneration. In summary, the HCD generated the metabolic and renal changes required for an obesity model, but with a delay in the development of these modifications concerning the HFD.

Oral supplementation with capsaicin reduces oxidative stress and IL-33 on a food allergy murine model.

BACKGROUND: Food allergy is an abnormal immune response to antigens introduced into the body through food. Its prevalence has increased in developed and developing countries. Natural products are traditionally used to alleviate and treat diseases, and diet can play a role in both the prevention and management of food allergy. The effects of capsaicin as an anti-oxidant, anticarcinogenic, and anti-inflammatory in the energy expenditure and suppression of fat accumulation have been demonstrated. This study evaluated the effect of oral supplementation with capsaicin on a food allergy model. METHODS: OVA-sensitized mice received ovalbumin solution, and they were fed with chow supplemented with capsaicin for 7 days. The control group received AIN-93 chow with no supplementation. IgE anti-ova, inflammatory infiltration, oxidative stress and metabolic analysis were performed. RESULTS: The results showed that capsaicin supplementation is not able to reduce characteristic signs of food allergy, such as production of IgE and weight loss. However, macrophages infiltration and IL-33 in proximal jejunum was reduced in OVA capsaicin group. In addition, hepatic triglycerides and intestinal hydroperoxides were reduced in both capsaicin groups. CONCLUSION: Oral supplementation with capsaicin attenuated important factors associated to food allergy such as inflammation and oxidative stress, suggesting better prognosis and evolution of the disease.

Fenofibrate prevents orotic acid--induced hepatic steatosis in rats.

The experiments performed in this report were designed to investigate the mechanisms involved in the metabolic alterations associated with orotic acid-induced hepatic steatosis and the effect of fenofibrate, a stimulant of peroxisome proliferators-activated receptor alpha (PPARalpha), on these alterations. Male Wistar rats were divided into three experimental groups: 1) fed a balanced diet (C); 2) fed a balanced diet supplemented with 1% orotic acid (OA); 3) fed OA diet containing 100 mg.kg(-1) bw.day(-1) fenofibrate (OA+F), for 9 days. Administration of OA to rats induced significant increase in the hepatic total lipids content, marked microvesicular steatosis and decrease in plasma lipids concentrations compared to control group. Fenofibrate treatment prevented fatty liver induction, caused an additional reduction on plasma lipids concentrations and caused a 40% decrease in the lipogenic rate in adipose tissue. The results also showed a 40% increase in lipoprotein lipase (LPL) activity in adipose tissue from OA treated group and fenofibrate administration induced a 50% decrease in LPL activity. The liver mRNA expression of PPARalpha and ACO (acyl CoA oxidase) were 85% and 68% decreased in OA group when compared to control, respectively. Fenofibrate treatment increased the PPARalpha and ACO expressions whereas the CPT-1 (carnitine palmitoyl transferase-1) expression was not altered. Our results have shown that fenofibrate treatment decreases the hepatic lipid content induced by OA which is mediated by an important increase in fatty acid oxidation consequent to an increase in hepatic mRNA expression of PPARalpha and ACO.

Improvement of the energy supply and contractile function in normal and ischemic rat hearts by dietary orotic acid.

AIMS: As cardiac performance is closely related to its energy supply, our study investigated the effect of the orotic acid cardioprotective agent on the pathways of energy supply, in both conditions of normal flow and ischemia. MAIN METHODS: Male Wistar rats were fed during nine days with a balanced diet only or supplemented with 1% orotic acid. KEY FINDINGS: Dietary administration of orotic acid increased the cardiac utilization of fatty acids, activity of the lipoprotein lipase, expression of the gene of peroxisome proliferator-activated receptor α and its target enzymes. In addition, orotic acid increased the myocardial uptake and incorporation of glucose, glycogen content and level of GLUT4, concentration of glycolytic metabolites and lactate production in both experimental conditions, baseline and after regional ischemia. SIGNIFICANCE: Thus, in orotic acid hearts there was a simultaneous stimulus of fatty acid oxidation and glycolytic pathway, reflected in increased energetic content even in pre-ischemia. The analysis of the cardiac contractility index showed a positive inotropic effect of orotic acid due, at least in part, to the increased availability of energy. The result allows us to suggest that the metabolic changes induced by orotic acid result in appreciable alterations on myocardial contractile function.

High-carbohydrate diet selectively induces tumor necrosis factor-α production in mice liver.

Obesity may represent a state of chronic low-grade inflammation associated with infiltration of adipose tissue by inflammatory cells. Tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1/JE), two important inflammatory cytokines, have been shown to be regulated according to changes in body adiposity. In this study on Swiss mice, we compared the influences of long-term high-carbohydrate (HC) or high-fat (HF) diet on adiposity, glucose tolerance, and secretion of TNF-α and MCP-1/JE by adipose tissue and liver. For 8 weeks, male Swiss mice (7-8 weeks) were fed either standard laboratory rodent diet (control group), HC diet (64% carbohydrate, 19% protein, and 11% fat), or HF diet (45% carbohydrate, 17% protein, and 38% fat), with the latter two diets having no fiber. Oral glucose tolerance test, triacylglycerol (TAG) plasma concentration, and systemic or tissue levels of the two proinflammatory cytokines were determined. Body weight increased by approximately 20% in mice fed the experimental diets compared with mice fed the control diet. Systemically, the hypercaloric diets induced hyperglycemia with impairment in glucose tolerance, elevated circulating TAG levels, and increased plasma concentrations of TNF-α and MCP-1/JE. In the target organs (adipose tissue and liver), both diets increased MCP-1/JE levels. However, the HC diet, but not the HF diet, was able to increase TNF-α concentration in the liver. These results have shown that the nature of nutrients influences the type of proinflammatory cytokines in target organs and may contribute to the comorbidities of obesity.

Efeito da restriçäo alimentar intrauterina sobre a resposta serotonérgica hipotalâmica à ingestäo alimentar na prole adulta / Effect of intrauterine food restrition on the hypothalamic serotonergic response to food intake in the offspring of rtas

Existem evidências de que um ambiente alimentar adverso durante a vida intrauterma pode causar o que se convencionou chamar de "programação fetal do metabolismo". Esta hipótese preconiza uma origem fetal para as alterações que, perpetuando-se na vida adulta, determinariam a gênese de patologias como obesidade e suas complicações associadas. O sistema nervoso central exerce um complexo controle sobre a homeostase energética corporal. A serotonina hipotalâmica tem participação importante neste controle, através de seus efeitos de inibir a ingestão alimentar e estimular a termogênese. O presente estudo teve o objetivo de avaliar se uma restrição alimentar intrauterina afeta a fisiologia do sistema serotonérgico hipotalâmico na prole adulta. Ratas gestantes tiveram acesso livre ao alimento (grupo Controle) ou a apenas 50 por cento da ingestão das ratas controles durante as duas primeiras semanas de gestação (grupo Restrito). Na terceira semana de gestação e na lactação, as ratas R tiveram a alimentação pareada, recebendo 100 por cento da quantidade ingerida pelas ratas C. Aos 4 meses de idade, as ratas restritas não apresentaram nenhuma alteração da massa corporal, ingestão alimentar de 24 horas, glicemia e insulmemia basais. Entretanto a adiposidade corporal total das ratas restritas foi significantemente mais alta que a das ratas controles. Utilizando microdiálise, avaliamos a liberação de serotonma em resposta à ingestão de alimento, no núcleo ventromedial do hipotálamo. Observamos que as ratas restritas ingeriram mais alimento e que esta ingestão induziu uma liberação de serotonina mais acentuada que nas ratas controles, dado compatível com a existência de resistência à ação do neurotransmissor liberado. Os dados indicam que a restrição alimentar intrauterina foi capaz de causar alterações que se verificaram na vida adulta, indicando uma programação fetal. Uma possível baixa efetividade da serotonina liberada poderia contribuir para a geração de um excedente de energia, o qual seria depositado sob a forma de gordura